SMAD公司
免疫印迹
分子生物学
转化生长因子
化学
污渍
细胞外基质
增生性瘢痕
转化生长因子β
细胞生长
基质金属蛋白酶
信号转导
细胞生物学
生物化学
生物
解剖
基因
作者
Yun Li,Zhencheng Yu,Deyu Zhao,Dong Han
出处
期刊:Life Sciences
[Elsevier]
日期:2021-07-01
卷期号:277: 119483-119483
被引量:10
标识
DOI:10.1016/j.lfs.2021.119483
摘要
Exploring the effects of corilagin on hypertrophic scar (HS) and its underlying mechanisms. Human HS-derived fibroblasts (HSFs) were isolated and treated with corilagin. To investigate the effects of corilagin on HSFs, quantitative real time polymerase chain reaction (qRT-PCR), western blotting, wound healing, and immunofluorescence assays were performed. These effects were confirmed in a rabbit ear scar model by histological and immunohistochemical studies. Lastly, western blot assay was performed to detect the protein levels of several components of the transforming growth factor (TGF)-β/Smad signaling pathway, as well as the protein levels of matrix metalloproteinases (MMPs) and tissue inhibitor of metalloproteinases (TIMPs). Corilagin showed multiple effects on HSFs, including does-dependent inhibition of collagen production, cell proliferation, and migration, besides suppression of the activation of HSFs. Moreover, corilagin suppressed HS formation and collagen deposition in a rabbit ear scar model. Corilagin also inhibited fibroblast proliferation and α-smooth muscle actin (α-SMA) expression in vivo. Finally, western blot analysis revealed that corilagin downregulated the protein levels of TGF-β1 and TGF-β receptor type I (TGFβRI), thus lowering the level of p-smad2/3, also affected the protein levels of MMPs and TIMP1. Corilagin could be a potential agent for HS treatment through the inhibition of extracellular matrix (ECM) deposition and multiple functions of fibroblasts.
科研通智能强力驱动
Strongly Powered by AbleSci AI